result 1043 件
JaLCDOI | 10.18926/AMO/48565 |
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FullText URL | 66_3_253.pdf |
Author | Zhang, Kai| Yamamoto, Yumiko| Suzuki, Tomonori| Yokota, Kenji| Ma, Shaobo| Nengah Dwi Fatmawati, Ni| Oguma, Keiji| |
Abstract | Cultured Clostridium botulinum strains produce progenitor toxins designated as 12S, 16S, and 19S toxins. The 12S toxin consists of a neurotoxin (NTX, 7S) and a non-toxic non-hemagglutinin (NTNH). The 16S and 19S toxins are formed by conjugation of the 12S toxin with hemagglutinin (HA), and the 19S toxin is a dimer of the 16S toxin. Type A cultures produce all 3 of these progenitor toxins, while type E produces only the 12S toxin. The 7S toxin is cleaved into heavy (H) and light (L) chains by a protease(s) in some strains, and the H chain has 2 domains, the N-terminus (Hn) and C-terminus (Hc). It has been reported that type A toxins bind to the intestinal cells or cultured cells via either HA or Hc. In this study, we investigated the binding of type A and E toxins to Caco-2 cells using Western blot analysis. Both the type E 7S and 12S toxins bound to the cells, with the 7S toxin binding more strongly, whereas, in the type A strain, only the 16S/19S toxins showed obvious binding. Pre-incubation of the type E 7S toxin with IgG against recombinant type E Hc significantly inhibited the 7S toxin binding, indicating that Hc might be a main binding domain of the type E toxin. |
Keywords | Clostridum botulinum neurotoxins Caco-2 binding Hc |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2012-06 |
Volume | volume66 |
Issue | issue3 |
Publisher | Okayama University Medical School |
Start Page | 253 |
End Page | 261 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2012 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 22729106 |
Web of Science KeyUT | 000305669700009 |
Related Url | http://ousar.lib.okayama-u.ac.jp/metadata/48451 |
JaLCDOI | 10.18926/AMO/48560 |
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FullText URL | 66_3_213.pdf |
Author | Kataoka, Masaki| Kunisada, Toshiyuki| Tanaka, Masato| Takeda, Ken| Itani, Satoru| Sugimoto, Yoshihisa| Misawa, Haruo| Senda, Masuo| Nakahara, Shinnosuke| Ozaki, Toshifumi| |
Abstract | There are a variety of treatment options for patients with spinal metastasis, and predicting prognosis is essential for selecting the proper treatment. The purpose of the present study was to identify the significant prognostic factors for the survival of patients with spinal metastasis. We retrospectively reviewed 143 patients with spinal metastasis. The median age was 61 years. Eleven factors reported previously were analyzed using the Cox proportional hazards model:gender, age, performance status, neurological deficits, pain, type of primary tumor, metastasis to major organs, previous chemotherapy, disease-free interval before spinal metastasis, multiple spinal metastases, and extra-spinal bone metastasis. The average survival of study patients after the first visit to our clinic was 22 months. Multivariate survival analysis demonstrated that type of primary tumor (hazard ratio [HR]=6.80, p<0.001), metastasis to major organs (HR=2.01, p=0.005), disease-free interval before spinal metastasis (HR=1.77, p=0.028), and extra-spinal bone metastasis (HR=1.75, p=0.017) were significant prognostic factors. Type of primary tumor was the most powerful prognostic factor. Other prognostic factors may differ among the types of primary tumor and may also be closely associated with primary disease activity. Further analysis of factors predicting prognosis should be conducted with respect to each type of primary tumor to help accurately predict prognosis. |
Keywords | spine metastasis survival prognostic factor cancer |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2012-06 |
Volume | volume66 |
Issue | issue3 |
Publisher | Okayama University Medical School |
Start Page | 213 |
End Page | 219 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2012 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 22729101 |
Web of Science KeyUT | 000305669700004 |
JaLCDOI | 10.18926/AMO/48262 |
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FullText URL | 66_2_119.pdf.pdf |
Author | Oka, Hiroaki| Ouchida, Mamoru| Kondo, Takuya| Morita, Fumio| Shimizu, Kenji| |
Abstract | Human lymphoblastoid TK6 and WTK-1 cells are widely used to detect mutagens in vitro. TK6 cells have wild-type TP53 alleles, while WTK-1 cells have one allele of mutated TP53. Both cells were treated with 5-fluorouracil (5-FU), and gene mutation assay and micronucleus assay were performed to clarify the differential response related to the TP53 gene status. The effects of 5-FU on gene expression were assessed by microarray and quantitative RT-PCR analyses. In WTK-1 cells, 5-FU increased the frequency of cells with micronucleus and mutation. In TK6 cells, frequency of cells with micronucleus was increased but the mutation frequency was not. The cytotoxicity induced by 5-FU was more prominent in TK6 cells than in WTK-1 cells. Analysis of gene expression showed that the genes involved in the TP53 pathway were up-regulated in TK6 cells but not in WTK-1 cells. The differential responses to 5-FU between these cell lines appeared to be due to the difference in the TP53 gene status, thus providing a molecular basis for the bioassays using these cell lines in the toxicology field. Our results indicate that the clinical efficacy of 5-FU chemotherapy may depend on the TP53 genotype. |
Keywords | 5-fluorouracil TP53 Tk mutation assays microarray analysis |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2012-04 |
Volume | volume66 |
Issue | issue2 |
Publisher | Okayama University Medical School |
Start Page | 119 |
End Page | 129 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2012 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 22525470 |
Web of Science KeyUT | 000303175300005 |
JaLCDOI | 10.18926/AMO/48076 |
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FullText URL | 66_1_7.pdf |
Author | Kawauchi, Keiichiro| Watanabe, Masami| Kaku, Haruki| Huang, Peng| Sasaki, Kasumi| Sakaguchi, Masakiyo| Ochiai, Kazuhiko| Huh, Nam-ho| Nasu, Yasutomo| Kumon, Hiromi| |
Abstract | The preclinical safety and therapeutic efficacy of adenoviral vectors that express the REIC/Dkk-3 tumor suppressor gene (Ad-REIC) was examined for use in prostate cancer gene therapy. The Ad-human (h) and mouse (m) REIC were previously demonstrated to induce strong anti-cancer effects in vitro and in vivo, and we herein report the results of two in vivo studies. First, intra-tumor Ad-hREIC administration was examined for toxicity and therapeutic effects in a subcutaneous tumor model using the PC3 prostate cancer cell line. Second, intra-prostatic Ad-mREIC administration was tested for toxicity in normal mice. The whole-body and spleen weights, hematological and serum chemistry parameters, and histological evaluation of tissues from throughout the body were analyzed. Both experiments indicated that there was no significant difference in the examined parameters between the Ad-REIC-treated group and the control (PBS- or Ad-LacZ-treated) group. In the in vitro analysis using PC3 cells, a significant apoptotic effect was observed after Ad-hREIC treatment. Confirming this observation, the robust anti-tumor efficacy of Ad-hREIC was demonstrated in the in vivo subcutaneous prostate cancer model. Based on the results of these preclinical experiments, we consider the adenovirus-mediated REIC/Dkk-3 in situ gene therapy to be safe and useful for the clinical treatment of prostate cancer. |
Keywords | REIC Dickkopf-3 gene therapy prostate cancer preclinical study |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2012-02 |
Volume | volume66 |
Issue | issue1 |
Publisher | Okayama University Medical School |
Start Page | 7 |
End Page | 16 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2012 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 22358134 |
Web of Science KeyUT | 000300800700002 |
JaLCDOI | 10.18926/AMO/47265 |
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FullText URL | 65_6_395.pdf |
Author | Harada, Sosuke| Sato, Shuhei| Suzuki, Etsuji| Okumura, Yoshihiro| Hiraki, Takao| Gobara, Hideo| Mimura, Hidefumi| Kanazawa, Susumu| Kaji, Mitsumasa| Fujiwara, Toshiyoshi| |
Abstract | The aim of the present study was to assess the diagnostic usefulness of Fluorine-18 fluorodeoxyglucose (18F-FDG) positron emission tomography/computed tomography (PET/CT) in the prediction of local recurrence of malignant lung tumors by analyzing the pre-radiofrequency ablation (RFA) maximal standardized uptake value (SUVmax). We performed a historical cohort study of consecutive malignant lung tumors treated by RFA from January 2007 to May 2008 at Okayama University Hospital. We selected only lung tumors examined by PET/CT within 90 days before RFA and divided them (10 primary and 29 metastatic) into 3 groups according to their tertiles of SUVmax. We calculated recurrence odds ratios in the medium group and the high group compared to the low group using multivariate logistic analysis. After we examined the relationship between SUVmax and recurrence in a crude model, we adjusted for some factors. Tumors with higher SUVmax showed higher recurrence odds ratios (medium group;1.84, high group;4.14, respectively). The tumor size also increased the recurrence odds ratio (2.67);we thought this was mainly due to selection bias because we excluded tumors less than 10mm in diameter. This study demonstrated the pre-RFA SUVmax in PET/CT may be a prognostic factor for local recurrence of malignant lung tumors. |
Keywords | fluorodeoxyglucose (FDG) positron emission tomography (PET) standardized uptake value (SUV) radiofrequency ablation (RFA) lung |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2011-12 |
Volume | volume65 |
Issue | issue6 |
Publisher | Okayama University Medical School |
Start Page | 395 |
End Page | 402 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2011 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 22189480 |
Web of Science KeyUT | 000298516900006 |
JaLCDOI | 10.18926/AMO/47013 |
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FullText URL | 65_5_315.pdf |
Author | Wang, Lei| Kaku, Haruki| Huang, Peng| Xu, Kexin| Yang, Kai| Zhang, Jiheng| Li, Ming| Xie, Liping| Wang, Xiaofeng| Sakai, Akiko| Watanabe, Masami| Nasu, Yasutomo| Shimizu, Kenji| Kumon, Hiromi| Na, Yanqun| |
Abstract | Deficiencies in the human DNA repair gene WRN are the cause of Werner syndrome, a rare autosomal recessive disorder characterized by premature aging and a predisposition to cancer. This study evaluated the association of WRN Leu1074Phe (rs1801195), a common missense single nucleotide polymorphism in WRN, with prostate cancer susceptibility in Chinese subjects. One hundred and forty-seven prostate cancer patients and 111 male cancer-free control subjects from 3 university hospitals in China were included. Blood samples were obtained from each subject, and the single nucleotide polymorphism WRN Leu1074Phe was genotyped by using a Snapshot assay. The results showed that WRN Leu1074Phe was associated with the risk of prostate cancer in Chinese men and that the TG/GG genotype displayed a decreased prevalence of prostate cancer compared with the TT genotype (OR=0.58, 95%CI:0.35-0.97, p=0.039). Through stratified analysis, more significant associations were revealed for the TG/GG genotype in the subgroup with diagnosis age <_ 72 yr (OR=0.27, 95%CI:0.12-0.61, p=0.002) and in patients with localized diseases (OR=0.36, 95%CI:0.19-0.70, p=0.003). However, no statistically significant difference was found in the subgroup with age >72 yr or in patients with advanced diseases. We concluded that the genetic variant Leu1074Phe in the DNA repair gene WRN might play a role in the risk of prostate cancer in Chinese subjects. |
Keywords | polymorphism prostatic neoplasms single nucleotide susceptibility WRN |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2011-10 |
Volume | volume65 |
Issue | issue5 |
Publisher | Okayama University Medical School |
Start Page | 315 |
End Page | 323 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2011 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 22037267 |
Web of Science KeyUT | 000296116400005 |
JaLCDOI | 10.18926/AMO/47011 |
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FullText URL | 65_5_299.pdf |
Author | Itani, Miki| Yamamoto, Yuji| Doi, Yusuke| Miyaishi, Satoru| |
Abstract | Postmortem degradation of DNA was quantitatively estimated. Brain, liver, kidney and muscle samples were obtained from sacrificed rats left at 20℃ or 4℃. The quantity of DNA was measured by real-time PCR using a primer set for a sequence in the Rsrc 1 gene. When the quantity of amplified DNA using 10ng Human Genomic DNA was defined as 100 RFU, the quantities in the brain, liver, kidney and skeletal muscle (each 2μg of dry weight) on the day of sacrifice were 253±11, 338±22, 556±14 and 531±12 Relative Fluorescence Units (RFU), respectively (mean±S.E., n=5). The quantity of amplified DNA decreased to below 10 RFU in 1-3 weeks in the liver, kidney and skeletal muscle at 20℃, while that in the brain was more than 10 RFU for six weeks, demonstrating the usefulness of the brain as a sample for DNA analysis of decaying corpses. It was suggested that quantifying the amplified DNA in the brain at 20℃ and in the liver at 4℃ as well as the ratio of the quantity of amplified DNA in the liver to the brain at 4℃ might be useful for diagnosing time of death. This study provides the first quantitative analysis of the postmortem progress of DNA degradation in the corpse. |
Keywords | DNA degradation postmortem interval personal identification |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2011-10 |
Volume | volume65 |
Issue | issue5 |
Publisher | Okayama University Medical School |
Start Page | 299 |
End Page | 306 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2011 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 22037266 |
Web of Science KeyUT | 000296116400003 |
JaLCDOI | 10.18926/AMO/46851 |
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FullText URL | 65_4_259.pdf |
Author | Ogata, Yoshiko| Aoe, Keisuke| Hiraki, Akio| Murakami, Kazuo| Kishino, Daizo| Chikamori, Kenichi| Maeda, Tadashi| Ueoka, Hiroshi| Kiura, Katsuyuki| Tanimoto, Mitsune| |
Abstract | The objective of this study was to evaluate the utility of the determination of adenosine deaminase (ADA) level in pleural fluid for the differential diagnosis between tuberculous pleural effusion (TPE) and malignant pleural effusion (MPE) in Japan, a country with intermediate incidence of tuberculosis (TB). We retrospectively reviewed the clinical records of 435 patients with pleural effusion and investigated their pleural ADA levels as determined by an auto analyzer. ROC analysis was also performed. The study included patients with MPE (n=188), TPE (n=124), benign nontuberculous pleural effusion (n=94), and pleural effusion of unknown etiology (n=29). The median ADA level in the TPE group was 70.8U/L, which was significantly higher than that in any other groups (p<0.05). The area under the curve (AUC) in ROC analysis was 0.895. With a cut-off level for ADA of 36U/L, the sensitivity, specificity, positive predictive value, and negative predictive value were 85.5%, 86.5%, 69.7%, and 93.6%, respectively. As many as 9% of patients with lung cancer and 15% of those with mesothelioma were false-positive with this ADA cutoff setting. Although the ADA activity in pleural fluid can help in the diagnosis of TPE, it should be noted that some cases of lung cancer or mesothelioma show high ADA activity in geographical regions with intermediate incidence of TB, in contrast to high prevalence areas. |
Keywords | pleural effusion adenosine deaminase tuberculosis lung cancer mesothelioma |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2011-08 |
Volume | volume65 |
Issue | issue4 |
Publisher | Okayama University Medical School |
Start Page | 259 |
End Page | 263 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2011 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 21860532 |
Web of Science KeyUT | 000294236700006 |
JaLCDOI | 10.18926/AMO/46850 |
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FullText URL | 65_4_247.pdf |
Author | Watanabe, Naomi| Shikata, Kenichi| Shikata, Yasushi| Sarai, Kei| Omori, Kazuyoshi| Kodera, Ryo| Sato, Chikage| Wada, Jun| Makino, Hirofumi| |
Abstract | Inflammatory processes are involved in the pathogenesis of diabetic nephropathy. The aim of this study was to clarify the role of mitogen-activated protein kinase (MAPK) pathways for induction of intercellular adhesion molecule-1 (ICAM-1) expression in glomerular endothelial cells under diabetic conditions. We examined the expression of ICAM-1 in the kidneys of experimental diabetic rats. Human glomerular endothelial cells (GE cells) were exposed to normal glucose concentration, high glucose concentration (HG), or high mannitol concentration (HM), and then the expression of the ICAM-1 protein and the phosphorylation of the 3 subfamilies of mitogen-activated protein kinase (MAPK) were determined using Western blot analysis. Next, to evaluate the involvement of MAPKs in HG- or HM-induced ICAM-1 expression, we preincubated GE cells with the inhibitors for ERK, p38 or JNK 1h prior to the application of glucose or mannitol. Expression of ICAM-1 was increased in the glomeruli of diabetic rats. Both HG and HM induced ICAM-1 expression and phosphorylation of ERK1/2, p38 and JNK in GE cells. Expression of ICAM-1 was significantly attenuated by inhibitors of ERK, p38 and JNK. We conclude that activation of ERK1/2, p38 and JNK cascades may be involved in ICAM-1 expression in glomerular endothelial cells under diabetic conditions. |
Keywords | diabetic nephropathy ICAM-1 ERK p38 MAPK JNK |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2011-08 |
Volume | volume65 |
Issue | issue4 |
Publisher | Okayama University Medical School |
Start Page | 247 |
End Page | 257 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2011 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 21860531 |
Web of Science KeyUT | 000294236700005 |
Author | Akiyama, Mari| Kobayashi, Katsuhiro| Yoshinaga, Harumi| Ohtsuka, Yoko| |
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Published Date | 2011-08-01 |
Publication Title | 岡山医学会雑誌 |
Volume | volume123 |
Issue | issue2 |
Content Type | Journal Article |
JaLCDOI | 10.18926/AMO/46628 |
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FullText URL | 65_3_169.pdf |
Author | Takeda, Masanori| Nagasaka, Takeshi| Dong-Sheng, Sun| Nishie, Hiroyuki| Oka, Tetsuhiro| Yamada, Eiji| Mori, Yoshiko| Shigeyasu, Kunitoshi| Morikawa, Tatsuya| Mizobuchi, Satoshi| Fujiwara, Toshiyoshi| |
Abstract | Secreted frizzled-related protein 2, (SFRP2) is a Wnt inhibitor whose promoter CpGs were recently found to be methylated at high frequency in colorectal cancers (CRCs). We hypothesized that the pattern of SFRP2 methylation may differ throughout the promoter during progressive tumorigenesis. Using combined bisulfite restriction analysis (COBRA), two methylation-sensitive regions (Regions A and B) of the SFRP2 promoter were investigated in 569 specimens of colorectal tissue:222 CRCs, 103 adenomatous polyps (APs), 208 normal colonic mucosa from CRC patients (N-Cs), and 36 normal colonic mucosa from subjects with no evidence of colorectal neoplasia at colonoscopy (N-Ns). Extensive (including both Regions A and B) and partial (either Region A or B) SFRP2 methylation levels were found in 61.7% and 24.8% of CRCs, 8.7% and 37.9% of APs, 3.9% and 39.9% of N-Cs, and 0% and 30.6% of N-Ns, respectively. Extensive methylation of the SFRP2 promoter was present primarily in CRCs, while partial methylation was common in APs. Whereas APs with the KRAS mutant showed no correlation to any pattern of SFRP2 methylation, extensive methylation of the SFRP2 promoter was significantly associated with KRAS mutant CRCs (p<.0001), suggesting that genetic alteration in the RAS-RAF pathway might precede the spread of CpG methylation through the SFRP2 promoter, which is observed in over 60% of advanced colorectal tumors. |
Keywords | BRAF/KRAS mutations promoter methylation colorectal cancer |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2011-06 |
Volume | volume65 |
Issue | issue3 |
Publisher | Okayama University Medical School |
Start Page | 169 |
End Page | 177 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2011 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 21709714 |
Web of Science KeyUT | 000292017500003 |
JaLCDOI | 10.18926/AMO/45274 |
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FullText URL | 65_2_143.pdf |
Author | Kobayashi, Yasuyuki| Saika, Takashi| Manabe, Daisuke| Nasu, Yasutomo| Kumon, Hiromi| |
Abstract | We analyzed the prognostic factors influencing survival after surgeries for upper urinary tract urothelial carcinoma (UUT-UC) with longer follow-up periods than in previous studies. Between January 2000 and December 2004, 386 patients underwent nephroureterectomy for UUT-UC. The data for the 221 patients with UUT-UC were retrospectively reviewed. Nine variables were evaluated for association with the survival outcomes of cause-specific survival. The prognostic significance was tested univariately with the log-rank test. The simultaneous effects of multiple prognostic factors were estimated by multiple regression analysis using the Cox proportional hazards model. The median follow-up was 38.4 months. The 5-year over all survival was 62.3%. Significant prognostic factors for disease-specific survival rate on univariate analysis were pathological stage (p0.0001), tumor grade (p0.0324), and venous invasion (p0.0001). Multivariate analysis revealed that only venous invasion was significant for disease-specific survival rate (p0.0205). Venous invasion was the only independent prognostic factor in pathologically localized UUT-UC. |
Keywords | nephroureterectomy transitional cell carcinoma upper urinary tract |
Amo Type | Corrected and Republished Article |
Publication Title | Acta Medica Okayama |
Published Date | 2011-04 |
Volume | volume65 |
Issue | issue2 |
Publisher | Okayama University Medical School |
Start Page | 143 |
End Page | 149 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2011 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 20200581 |
Web of Science KeyUT | 000289818800011 |
JaLCDOI | 10.18926/AMO/45270 |
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FullText URL | 65_2_113.pdf |
Author | Morikawa, Toshio| Yamamoto, Yuji| Miyaishi, Satoru| |
Abstract | We have developed a new method for sex determination based on simultaneous detection of the SRY (sex-determining region Y), STS (steroid sulfatase) and amelogenin (AMELX and AMELY) gene regions and their homologous sequences. The sex of 246 blood samples was correctly determined by this method. An AMELY-deleted male sample, which would have been erroneously considered female based solely on analysis of the amelogenin locus, was successfully identified as male by the present method. The detection limit of this method was 63 pg of genomic DNA, and the male DNA component could be detected from mixed samples having a male:female ratio as low as 1:10. This method was useful for degraded DNA and possessed the human specificity. Practical application to 35 autopsy cases is described. |
Keywords | sex determination SRY (sex-determining region Y) multiplex PCR forensic casework |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2011-04 |
Volume | volume65 |
Issue | issue2 |
Publisher | Okayama University Medical School |
Start Page | 113 |
End Page | 122 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2011 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 21519369 |
Web of Science KeyUT | 000289818800007 |
JaLCDOI | 10.18926/AMO/45266 |
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FullText URL | 65_2_81.pdf |
Author | Sasaki, Motofumi| Shikata, Kenichi| Okada, Shinichi| Miyamoto, Satoshi| Nishishita, Shingo| Usui Kataoka, Hitomi| Sato, Chikage| Wada, Jun| Ogawa, Daisuke| Makino, Hirofumi| |
Abstract | Glomerular hyperfiltration is a common pathway leading to glomerulosclerosis in various kinds of kidney diseases. The 5/6 renal ablation is an established experimental animal model for glomerular hyperfiltration. On the other hand, low-grade inflammation is also a common mechanism for the progression of kidney diseases including diabetic nephropathy and atherosclerosis. Here we analyzed the gene expression profile in the remnant kidney tissues of 5/6 nephrectomized mice using a DNA microarray system and compared it with that of sham-operated control mice. The 5/6 nephrectomized mice showed glomerular hypertrophy and an increase in the extracellular matrix in the glomeruli. DNA microarray analysis indicated the up-regulated expression of various kinds of genes related to the inflammatory process in remnant kidneys. We confirmed the up-regulated expression of platelet factor-4, and monocyte chemoattractant protein-1, 2, and 5 in remnant kidneys by RT-PCR. The current results suggest that the inflammatory process is involved in the progression of glomerulosclerosis and is a common pathway of the pathogenesis of kidney disease. |
Keywords | kidney inflammation chemokine |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2011-04 |
Volume | volume65 |
Issue | issue2 |
Publisher | Okayama University Medical School |
Start Page | 81 |
End Page | 89 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2011 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 21519365 |
Web of Science KeyUT | 000289818800003 |
Author | Noma, Kazuhiro| Tanakaya, Kohji| Takeuchi, Hitoshi| Konaga, Eiji| Fujiwara, Toshiyoshi| |
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Published Date | 2011-04-01 |
Publication Title | 岡山医学会雑誌 |
Volume | volume123 |
Issue | issue1 |
Content Type | Journal Article |
Author | Yamada, Hiroshi| Padilla-Parra, Sergi| Park, Sun Joo| Itoh, Toshiki| Chaineau, Mathilde| Monaldi, Ilaria| Cremona, Ottavio| Benfenati, Fabio| Camilli, Pietro De| Coppey-Moisan, Maïté| Tramier, Marc| Galli, Thierry| Takei, Kohji| |
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Published Date | 2011-04-01 |
Publication Title | 岡山医学会雑誌 |
Volume | volume123 |
Issue | issue1 |
Content Type | Journal Article |
JaLCDOI | 10.18926/AMO/43829 |
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FullText URL | 65_1_41.pdf |
Author | Tokumori, Kimihiko| Wang, Da-Hong| Takigawa, Tomoko| Takaki, Jiro| Ogino, Keiki| |
Abstract | This study aimed to determine whether there was any association between the regional climate and the proportion of people with joint pain. Regional climate data between 1971 and 2000 were obtained from the Japan Meteorological Agency. The variables used in the cluster analysis included sunlight hours, amount of precipitation, number of days with precipitation, and temperature. The regional proportion of people with joint pain was obtained from the National Survey for Health in 2001. After performing a cluster analysis, one-way ANOVA and Welch's test were used to determine whether the climate characteristics of the clusters were significantly different. Within each cluster, stepwise multiple linear regression analyses were performed. We found that sunlight hours showed a direct, negative association with the proportion of people with joint pain (adjusted R2=0.532, p=0.016) in cluster 1, which was characterized as the region with the fewest total hours of sunlight, less precipitation, a modest number of rainy days, and low temperature. In the other clusters, the regional female population rate (cluster 2) and the senior population rate (cluster 3, 4) were the primary predictors. We concluded that the degree of exposure to sunlight may play a crucial role in prevention of joint pain. This finding should encourage people to set aside some time for staying outdoors in their daily lives. |
Keywords | climate joint pain sunlight hours cluster analysis |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2011-02 |
Volume | volume65 |
Issue | issue1 |
Publisher | Okayama University Medical School |
Start Page | 41 |
End Page | 48 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2011 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 21339795 |
Web of Science KeyUT | 000287620500006 |
JaLCDOI | 10.18926/AMO/40133 |
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FullText URL | 64_4_249.pdf |
Author | Masumoto, Akio| Masuyama, Hisashi| Takamoto, Norio| Akahori, Yoichiro| Hiramatsu, Yuji| |
Abstract | It has been reported that prolactin (PRL) is cleaved to 14 or 16 kDa fragments by cathepsin D in vitro and in vivo, and that such fragments exhibit antiangiogenic and proapoptotic properties. The aim of this study was to investigate the relationship between pregnancy induced hypertension (PIH) and the placental expression of antiangiogenic PRL fragments and cathepsin D. Placental expression of PRL fragments and cathepsin D was evaluated by Western blot analysis in a group of 9 pregnant women consisting of 5 normal pregnancies and 4 severe PIH cases. Antiangiogenic PRL fragments were detected in 4 placental samples from all PIH cases but not detected in those from normal pregnancies (p0.05). The expression of cathepsin D in PIH placentas was significantly lower than that in those without PIH (p0.05), while the placental expression of procathepsin D was significantly greater in PIH cases than in the normal pregnancies (p0.05). These data suggest that antiangiogenic PRL fragments in the placenta may be present only in PIH cases, and that PRL fragments in the placenta might be implicated in the pathophysiology of PIH. |
Keywords | pregnancy induced hypertension preeclampsia prolactin prolactin fragment cathepsin-D |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2010-08 |
Volume | volume64 |
Issue | issue4 |
Publisher | Okayama University Medical School |
Start Page | 249 |
End Page | 255 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 20802542 |
Web of Science KeyUT | 000281384400006 |
Author | Fujiwara, Kazuo| Endo, Hirosuke| Miyake, Yoshiaki| Ozaki, Toshifumi| |
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Published Date | 2010-08-02 |
Publication Title | 岡山医学会雑誌 |
Volume | volume122 |
Issue | issue2 |
Content Type | Journal Article |
Author | Nagasaka, Takeshi| Tanaka, Noriaki| Sun, Dong-Sheng| Naomoto, Yoshio| Mastubara, Nagahide| Yagi, Takahito| Fujiwara, Toshiyoshi| |
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Published Date | 2010-08-02 |
Publication Title | 岡山医学会雑誌 |
Volume | volume122 |
Issue | issue2 |
Content Type | Journal Article |